Summary
Highlights
Sporozoans are classified under the group Epicomplexa, sharing features like an apical complex for host cell invasion. They are obligate intracellular parasites, lack locomotion, and depend on blood flow, host cells, or vectors. Their life cycle includes sexual (sporogony) and asexual (schizogony) reproduction. Plasmodium, the parasite causing malaria, is transmitted by mosquitoes and remains a leading cause of parasitic mortality, especially in tropical countries. Four main species infect humans: P. falciparum, P. vivax, P. ovale, and P. malariae, with P. falciparum and P. vivax accounting for over 90% of cases. P. falciparum is common in the Philippines and P. vivax is the most widespread globally. Mixed infections can occur, leading to severe symptoms. Common antimalarial drugs include chloroquine and mepacrine, and the primary vector is the female Anopheles minimus variant flavirostris mosquito.
The asexual cycle (schizogony) occurs in humans, who serve as intermediate hosts. The infective stage for humans is the sporozoite, injected by an infected mosquito. Sporozoites travel to the liver, entering hepatocytes and multiplying to form merozoites. This is the exoerythrocytic cycle, a silent stage where the parasites multiply in liver cells before emerging as merozoites. These merozoites then invade circulating red blood cells, developing into ring trophozoites, then mature trophozoites, and finally schizonts. Schizonts rupture, releasing more merozoites to infect new red blood cells, continuing the erythrocytic cycle. The rupture of infected red blood cells releases toxins, causing characteristic fever, chills, and sweating. Some merozoites develop into gametocytes (micro- and macro-), which are crucial for the next stage of the life cycle.
The sexual cycle (sporogony) takes place in the female Anopheles mosquito, the definitive host. The mosquito becomes infected by ingesting gametocytes from an infected human's blood. In the mosquito's stomach, gametocytes mature into gametes, fuse to form a zygote, which then develops into a motile ookinete. The ookinete penetrates the gut wall, forming an oocyst. Inside the oocyst, numerous sporozoites are produced. These sporozoites migrate to the mosquito's salivary glands, ready to be injected into another human, thus completing the cycle.
Malaria is characterized by recurrent fever, chills, and sweating, caused by the synchronized rupture of infected red blood cells and the release of toxins. The fever patterns vary by Plasmodium species: every 36 hours for P. falciparum, every 48 hours for P. ovale and P. vivax, and every 72 hours for P. malariae. Continuous destruction of red blood cells leads to anemia and splenomegaly. P. falciparum is particularly fatal due to its ability to infect all red blood cell stages, leading to complications like cerebral malaria (sticky infected red blood cells blocking brain vessels, causing decreased oxygen and brain damage) and black water fever (massive intravascular hemolysis leading to hemoglobinuria and potential acute kidney failure).
Some individuals exhibit genetic resistance to malaria. For instance, Duffy antigen-negative individuals are resistant to P. vivax, while M and N blood group antigen-negative individuals are resistant to P. falciparum. G6PD deficiency and sickle cell trait also confer some resistance. Each Plasmodium species has distinct characteristics: P. vivax causes relapsing malaria due to dormant hypnozoites in the liver, infects reticulocytes, and often shows Schüffner’s dots. P. ovale also causes relapsing malaria due to hypnozoites, infects young red blood cells, and causes red blood cells to become oval-shaped with fimbriated edges. P. malariae causes long-lasting but milder infections, prefers older red blood cells, and distinctive band forms and 'rosette' schizonts. P. falciparum is the most dangerous, infecting all red blood cell stages, showing multiple ring forms in a single RBC, and crescent or banana-shaped gametocytes.
P. knowlesi is the fifth human malaria parasite, naturally infecting long-tailed macaques and transmitted to humans via zoonotic transmission. Laboratory diagnosis of malaria involves blood examinations such as thick and thin smears (for screening and quantification, respectively), and immunologic tests. Optimal acid tests detect parasite lactate dehydrogenase (LDH) produced by all Plasmodium species, while maloquil tests detect histidine-rich protein 2 (HRP-2) specific to P. falciparum.
Babesia microti is another parasitic infection that affects red blood cells, causing babesiosis (also known as Texas cattle fever or red water fever). It is spread by Ixodes ticks and can also be transmitted via blood transfusion. Similar to Plasmodium, Babesia causes red water fever due to extensive red blood cell breakdown, leading to dark red urine. However, Babesia differs from Plasmodium in that it lacks an exoerythrocytic (liver) stage, directly infecting red blood cells. Diagnostic features include tetrad forms (Maltese cross appearance) in red blood cells. Clinically, babesiosis symptoms are similar to malaria, presenting with high fever, myalgia, fatigue, and malaise. Co-infection with Lyme disease or human granulocytotropic anaplasmosis is not uncommon.